Aging of cells stopped?

Andreas John wrote:
This is probably what you have heard rumours about:
<quote from Science-Week>
10. EXTENSION OF MITOTIC LIMITS BY TELOMERASE EXPRESSION
Somatic cells are all cells other than germline cells such as egg
cells and sperm cells, and the term "cellular replicative
senescence" refers to the observation that somatic cells, in
contrast to germline cells, can proliferate (divide) only a fixed
number of times, the actual number dependent on the organism from
which the somatic cells derive. Since there is a general correl-
ation between cellular replicative senescence in vitro and the
average life-spans of various animals (including humans),
cellular replicative senescence has been implicated in aging and
age-related pathologies. Telomeres are regions at the ends of
chromosomes consisting of repeats of particular nucleotide
sequences, and with each somatic cell division a small part of
the telomere is ordinarily lost. What has been observed is that
in germline cells the lengths of telomeres are maintained
constant by repair, while in somatic cells this repair does not
occur, and this difference has led to the idea that the finite
proliferative capacity of somatic cells is related to the
ultimate depletion of telomere lengths. The enzyme telomerase is
the enzyme that causes repair of telomeres, and this enzyme is
active in germline cells, but it is not expressed in most somatic
cells. In animals, epithelial cells compose the cell layers that
form the interface between a tissue and the external environment,
for example, the cells of the skin, the lining of the intestinal
tract, and the lung airway passages, and fibroblasts are a type
of connective tissue cell that secret structured proteins such as
collagen. Transfection is the uptake of exogenous (foreign) DNA
fragments in solution directly into animals cells in laboratory
culture, and is one method of introducing foreign genes into
cells. The term "vector", in the context of DNA cloning, is any
DNA fragment used in a transfection process. ... ... Bodnar et al
(10 authors at 2 installations, US) now report that two normal
human cell types (retinal pigment epithelial cells and foreskin
fibroblasts) that do not ordinarily express telomerase, can be
transfected with vectors encoding the human telomerase catalytic
subunit, the transfected cells (as opposed to controls) then
exhibiting elongated telomeres, dividing vigorously and exceeding
their normal life-span by at least 20 doublings. The authors
suggest their results establish a causal relationship between
telomere shortening and in vitro cellular replicative senescence,
and that the ability to maintain normal human cells in a youthful
state can have important applications in research and medicine.
QY: Serge Lichtsteiner <slichtste at geron.com> (Science 16 Jan 98)
</quote from science week>
So they haven't quite stopped ageing but rather suggested a causal
relationship between telomere shortening and cellular replicative
senescence. That this is an important finding is obvious.
--
Venlig hilsen
Brian Bjørn
Stud.med., skolarstipendiat
http://www.mdb.ku.dk/bbjorn/